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BackgroundLowering lipid variability may be a potential strategy for improving the inflammatory state in patients with coronary heart disease (CHD). This study investigated the association between the variability of non-high-density lipoprotein cholesterol (non-HDL-C) and the neutrophil-to-lymphocyte ratio (NLR).MethodsThis study enrolled 2,711 CHD patients subjected to percutaneous coronary intervention (PCI). During the 1-year follow-up period after PCI, the variability of non-HDL-C was assessed using standard deviation (SD), coefficient of variation (CV), and variability independent of mean (VIM). NLR was calculated as the ratio of absolute neutrophil count to absolute lymphocyte count. The relationship between the non-HDL-C variability and the average NLR level during follow-ups was examined using a linear regression analysis.ResultsThe mean age of the patients was 64.4 ± 10.8 years, with 72.4% being male. The average NLR level was 2.98 (2.26–4.14) during the follow-up (1 year after PCI). The variability of non-HDL-C was 0.42 (0.26–0.67) for SD, 0.17 (0.11–0.25) for CV, and 0.02 (0.01–0.03) for VIM. A locally weighted scatterplot smoothing curve indicates that the average levels of NLR increased with increasing variability of non-HDL-C. Regardless of the variability assessment method used, non-HDL-C variability was significantly positively associated with the average NLR level during follow-ups: SD [β (95% CI) = 0.681 (0.366–0.996)], CV [β (95% CI) = 2.328 (1.458–3.197)], and VIM [β (95% CI) = 17.124 (10.532–23.715)]. This association remained consistent across subgroups stratified by age, gender, diabetes, and hypertension.ConclusionThe variability of non-HDL-C was positively associated with NLR in patients with CHD, suggesting that reducing non-HDL-C variability may improve the low-grade inflammatory state in CHD patients.

BackgroundCardiac dysfunction is a well-established risk factor for contrast-associated acute kidney injury (CA-AKI). Nevertheless, the relationship between cardiac remodeling, as assessed by echocardiography, and CA-AKI remains uncertain.MethodA total of 3,241 patients undergoing coronary angiography (CAG) with/without percutaneous coronary intervention (PCI) were enrolled in this retrospective study. Collected echocardiographic parameters were normalized by body surface area (BSA) and divided according to quartile, including the left ventricular internal end-diastolic diameter index (LVIDDI), left ventricular internal end-systolic diameter index (LVIDSI), and left ventricular mass index (LVMI). Logistic regression analysis was conducted to ascertain the association between structural parameter changes and CA-AKI. Further investigation was performed in different subgroups.ResultsThe mean age of the participants was 66.6 years, and 16.3% suffered from CA-AKI. LVIDSI [≥22.9 mm/m2: OR = 1.953, 95%CI (1.459 to 2.615), P 0.05). The presence of eccentric hypertrophy [OR = 1.400, 95%CI (1.093 to 1.793), P = 0.008] and the coexistence of hypertrophy and dilation [OR = 1.397, 95%CI (1.091 to 1.789), P = 0.008] carried a higher CA-AKI risk.ConclusionThe presence of cardiac remodeling, assessed by echocardiography, is associated with a higher risk of CA-AKI.

ObjectiveContrast-associated acute kidney injury (CA-AKI) is a critical complication when applying contrast medium, and the risk factors of CA-AKI have not been fully clarified. This study aimed to explore the relationships of CA-AKI with erythrocyte parameters, anemia conditions, and sex differences in patients after coronary angiography (CAG).MethodsIn this retrospective study, 4,269 patients who underwent CAG were enrolled. CA-AKI was defined as an increase in plasma creatinine of at least 0.5 mg/dl (44 μmol/L) or 25% within 72 h after exposure to the contrast medium. Three erythrocyte parameters, including hemoglobin, hematocrit, and red blood cell (RBC) count, were collected on admission. Logistic regression analyses were used to examine the associations of sex differences and erythrocyte parameters with CA-AKI in the overall population, restricted cubic splines to visualize these associations flexibly. Moreover, stratified and sensitivity analyses were conducted to assess the robustness of the findings.ResultsOverall, the mean (± standard deviations) age of patients was 67.05 ± 10.77 years, and 759 subjects (17.8%) developed CA-AKI. The results showed L-shaped relationships between erythrocyte parameters and CA-AKI incidence in each model (all P

ObjectiveThe prognostic significance of troponin elevation following percutaneous coronary intervention (PCI) remains debated. This study aimed to evaluate the association between different thresholds of post-PCI cardiac troponin I (cTnI) and mortality.MethodsFrom January 2012 to July 2017, 5,218 consecutive patients undergoing elective PCI with pre-PCI cTnI < 99th percentile of the upper reference limit (URL) were included. Levels of cTnI were measured before PCI and every 8 h for 24 h after procedural. The outcomes were 3-year cardiac mortality.ResultsPatients had a mean age of 66.2 years, 27.6% were women, 67.0% had hypertension, and 26.2% had diabetes mellitus. During the 3 years of follow-up, cardiac death occurred in 0.86%, 1.46%, 1.69%, 2.36%, and 2.86% of patients with cTnI < 1, ≥ 1 to < 5, ≥ 5 to < 35, ≥ 35 to < 70, and ≥ 70 times URL. The cardiac mortality rate was moderately increased with higher peak cTnI values, but the Kaplan–Meier curve demonstrated no significant association between any increment of cTnI and either cardiac or non-cardiac mortality. Isolated cTnI increment of ≥ 5 × URL, ≥ 35 × URL, and ≥ 70 × URL was occurred in 1,379 (26.4%), 197 (3.8%), and 70 (1.3%) patients, respectively. In multivariate Cox regression analysis and Fine-Gray model, none of the above cTnI thresholds was significantly associated with an increased risk of cardiac death.ConclusionIn patients who underwent elective PCI, post-PCI cTnI elevation is not independently associated with cardiac mortality.

BackgroundAcute exacerbation of chronic heart failure contributes to substantial increases in major adverse cardiovascular events (MACE). The study developed a risk score to evaluate the severity of heart failure which was related to the risk of MACE.MethodsThis single-center retrospective observational study included 5,777 patients with heart failure. A credible random split-sample method was used to divide data into training and validation dataset (split ratio = 0.7:0.3). Least absolute shrinkage and selection operator (Lasso) logistic regression was applied to select predictors and develop the risk score to predict the severity category of heart failure. Receiver operating characteristic (ROC) curves, and calibration curves were used to assess the model’s discrimination and accuracy.ResultsBody-mass index (BMI), ejection fraction (EF), serum creatinine, hemoglobin, C-reactive protein (CRP), and neutrophil lymphocyte ratio (NLR) were identified as predictors and assembled into the risk score (P < 0.05), which showed good discrimination with AUC in the training dataset (0.770, 95% CI:0.746–0.794) and validation dataset (0.756, 95% CI:0.717–0.795) and was well calibrated in both datasets (all P > 0.05). As the severity of heart failure worsened according to risk score, the incidence of MACE, length of hospital stay, and treatment cost increased (P < 0.001).ConclusionA risk score incorporating BMI, EF, serum creatinine, hemoglobin, CRP, and NLR, was developed and validated. It effectively evaluated individuals’ severity classification of heart failure, closely related to MACE.

BackgroundHeart failure (HF), primarily caused by conditions such as coronary heart disease or cardiomyopathy, is a global health problem with poor prognosis and heavy burden on healthcare systems. As biomarkers of myocardial injury and fibrosis, suppression of tumorigenicity 2 (ST2) and galectin-3 were recommended for prognosis stratification in HF guidelines. However, the causality between these two mediators and HF remains obscure. This study aimed to explore the causal relationship of genetically determined ST2 and galectin-3 with the risk of HF.MethodsWe used the two-sample Mendelian randomization (MR) method, incorporating available genome-wide association summary statistics, to investigate the causal association of ST2 and galectin-3 with HF risk. We applied inverse-variance weighted analysis as the main method of analysis.ResultsIn our final MR analysis, 4 single-nucleotide polymorphisms (SNPs) of ST2 and galectin-3, respectively, were identified as valid instrumental variables. Fixed-effect inverse variance weighted (IVW) analysis indicated that genetically predicted ST2 and galectin-3 were not causally associated with HF risk 3. [odds ratio (OR) = 0.9999, 95% confidence interval [CI] = 0.9994–1.0004, p = 0.73; OR = 1.0002, 95% CI = 0.9994–1.0010, p = 0.60, respectively]. These findings were robust in sensitivity analyses, including MR-Egger regression and leave-one-out analysis.ConclusionThis MR study provided no evidence for the causal effects of ST2 and galectin-3 on HF risk.

BackgroundIncreased plaque vulnerability and higher lipid variability are causes of adverse cardiovascular events. Despite a close association between glucose and lipid metabolisms, the influence of elevated glycated hemoglobin A1c (HbA1c) on plaque vulnerability and lipid variability remains unclear.MethodsAmong subjects undergoing percutaneous coronary intervention (PCI) from 2009 through 2019, 366 patients received intravascular optical coherence tomography (OCT) assessment and 4,445 patients underwent the scheduled follow-ups within 1 year after PCI. Vulnerability features of culprit vessels were analyzed by OCT examination, including the assessment of lipid, macrophage, calcium, and minimal fibrous cap thickness (FCT). Visit-to-visit lipid variability was determined by different definitions including standard deviation (SD), coefficient of variation (CV), and variability independent of the mean (VIM). Multivariable linear regression analysis was used to verify the influence of HbA1c on plaque vulnerability features and lipid variability. Exploratory analyses were also performed in non-diabetic patients.ResultsAmong enrolled subjects, the pre-procedure HbA1c was 5.90 ± 1.31%, and the average follow-up HbA1c was 5.98 ± 1.16%. By OCT assessment, multivariable linear regression analyses demonstrated that patients with elevated HbA1c had a thinner minimal FCT (β = −6.985, P = 0.048), greater lipid index (LI) (β = 226.299, P = 0.005), and higher macrophage index (β = 54.526, P = 0.045). Even in non-diabetic patients, elevated HbA1c also linearly decreased minimal FCT (β = −14.011, P = 0.036), increased LI (β = 290.048, P = 0.041) and macrophage index (β = 120.029, P = 0.048). Subsequently, scheduled follow-ups were performed during 1-year following PCI. Multivariable linear regression analyses proved that elevated average follow-up HbA1c levels increased the VIM of lipid profiles, including low-density lipoprotein cholesterol (β = 2.594, P < 0.001), high-density lipoprotein cholesterol (β = 0.461, P = 0.044), non-high-density lipoprotein cholesterol (β = 1.473, P < 0.001), total cholesterol (β = 0.947, P < 0.001), and triglyceride (β = 4.217, P < 0.001). The result was consistent in non-diabetic patients and was verified when SD and CV were used to estimate variability.ConclusionIn patients undergoing elective PCI, elevated HbA1c increases the atherosclerotic plaque vulnerability and the visit-to-visit variability of lipid profiles, which is consistent in non-diabetic patients.

Background: Metoprolol is the most used cardiac selective β-blocker and has been recommended as a mainstay drug in the management of acute myocardial infarction (AMI). However, the evidence supporting this regimen in periprocedural myocardial infarction (PMI) is limited.Methods: This study identified 860 individuals who suffered PMI following percutaneous coronary intervention (PCI) procedure and median followed up for 3.2 years. Subjects were dichotomized according to whether they received chronic oral sustained-release metoprolol succinate following PMI. After inverse probability of treatment weighting (IPTW) adjustment, logistic regression analysis, Kaplan-Meier curve, and Cox regression analysis were performed to estimate the effects of metoprolol on major adverse cardiovascular events (MACEs) which composed of cardiac death, myocardial infarction (MI), stroke, and revascularization. Moreover, an exploratory analysis was performed according to hypertension, cardiac troponin I (cTnI) elevation, and cardiac function. A double robust adjustment was used for sensitivity analysis.Results: Among enrolled PMI subjects, 456 (53%) patients received metoprolol treatment and 404 (47%) patients received observation. After IPTW adjustment, receiving metoprolol was found to reduce the subsequent 3-year risk of MACEs by nearly 7.1% [15 vs. 22.1%, absolute risk difference (ARD) = 0.07, number needed to treat (NNT) = 14, relative risk (RR) = 0.682]. In IPTW-adjusted Cox regression analyses, receiving metoprolol was related to a reduced risk of MACEs (hazard ratio [HR] = 0.588, 95%CI [0.385–0.898], P = 0.014) and revascularization (HR = 0.538, 95%CI [0.326–0.89], P = 0.016). Additionally, IPTW-adjusted logistic regression analysis showed that receiving metoprolol reduced the risk of MI at the third year (odds ratio [OR] = 0.972, 95% CI [0.948–997], P = 0.029). Exploratory analysis showed that the protective effect of metoprolol was more pronounced in subgroups of hypertension and cTnI elevation ≥1,000%, and was remained in patients without cardiac dysfunction. The benefits above were consistent when double robust adjustments were performed.Conclusion: In the real-world setting, receiving metoprolol treatment following PCI-related PMI has decreased the subsequent risk of MACEs, particularly the risk of recurrent MI and revascularization.

Background: Although several observational studies have shown an association between birth weight (BW) and atrial fibrillation (AF), controversy remains. In this study, we aimed to explore the role of elevated BW on the etiology of AF.Methods: A two-sample Mendelian randomization (MR) study was designed to infer the causality. The genetic data on the associations of single-nucleotide polymorphisms (SNPs) with BW and AF were separately obtained from two large-scale genome-wide association studies with up to 321,223 and 1,030,836 individuals, respectively. SNPs were identified at a genome-wide significant level (p